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Functional interaction between TRP4 and CFTR in mouse aorta endothelial cells.

L Wei¹, M Freichel, M Jaspers

¹Department of Physiology, Campus Gasthuisberg, KU Leuven, Leuven, Belgium. Wei.Lin@med.kuleuven.ac.be

|May 18, 2001

Summary

TRP4 channels are essential for activating cystic fibrosis transmembrane conductance regulator (CFTR) in mouse aorta endothelium. Without TRP4, CFTR-mediated currents are absent, suggesting TRP4 facilitates functional CFTR channel formation.

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Area of Science:

Endothelial cell biology
Ion channel function
Molecular interactions

Background:

Mouse aorta endothelium (MAEC) cells express transcripts for the cystic fibrosis transmembrane conductance regulator (CFTR).
TRP4, a putative Ca2+ channel, is investigated for its interaction with CFTR in MAEC.

Purpose of the Study:

To elucidate the functional interaction between TRP4 and CFTR in MAEC.
To determine the role of TRP4 in CFTR-mediated currents within the endothelium.

Main Methods:

Reverse transcription polymerase chain reaction (RT-PCR) to analyze gene expression.
Electrophysiological recordings to measure chloride currents.
Utilizing wild-type (trp4 +/+) and knockout (trp4 -/-) MAEC cells.

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Main Results:

MAEC cells express CFTR transcripts.
A phosphorylating cocktail activated a chloride current in wild-type MAEC with characteristics of CFTR-mediated currents.
This CFTR-like current was absent in trp4 -/- MAEC, despite unchanged CFTR expression.
Glibenclamide blocked the observed current, further supporting CFTR involvement.

Conclusions:

TRP4 is necessary for the activation of CFTR in the endothelium.
TRP4 may act as a scaffold, essential for the formation of functional CFTR channels in MAEC.